Bigelovin, a sesquiterpene lactone isolated from Inula helianthus-aquatica, is a selective retinoid X receptor α agonist. Bigelovin suppresses tumor growth through inducing apoptosis and autophagy via the inhibition of mTOR pathway regulated by ROS generation[1].
Bigelovin (0-20 μM, 24-72 h) significantly inhibits cell viability of liver cancer cells and induces apoptosis and autophagy[1].Bigelovin causes a significant increase of p62, LC3B-II, Beclin-1 and a corresponding decrease of p62 levels in a time-dependent manner[1].Bigelovin induces cell death involves the suppression of mTOR pathway regulated by ROS production[1]. Cell Viability Assay[1] Cell Line: HepG2 and SMMC-7721 cells.
Bigelovin (BigV, 5, 10, 20 mg/kg) exerts anti-tumor activity in HepG2 xenograft tumor model[1]. Animal Model: HepG2 xenograft model based on the male athymic BALB/c nude mice (5-6 weeks old, 18-22 g)[1].
[1]. Bei Wang, et al. Bigelovin, a sesquiterpene lactone, suppresses tumor growth through inducing apoptosis and autophagy via the inhibition of mTOR pathway regulated by ROS generation in liver cancer. Biochem Biophys Res Commun. 2018 May 5;499(2):156-163.